Experimental Fetal Anencephaly in the Rhesus Monkey: Effect on Gestational Length and Fetal and Maternal Plasma Steroids

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Abstract
Experimental fetal anencephaly was produced in 23 rhesus monkeys (Macaca mulatto) by removing the fetal head between days 73–82 of gestation. Timing of parturition was significantly disrupted in the 10 animals that were allowed to deliver vaginally: 3 of the anencephalic fetuses were born prematurely and 4 were born postmaturely. Pregnancies of the other 13 animals were interrupted by cesarean section between days 140–151 of gestation. Anencephalic fetuses were significantly lighter than control fetuses and their adrenal glands were atrophied. Mean amniotic fluid volumes and total placental weights of the anencephalic group were not statistically different from those of the control group. Experimental fetal anencephaly significantly decreased maternal venous estradiol; however, it did not affect the concentrations of cortisone, cortisol or estrone in the maternal saphenous vein, fetal umbilical vein or umbilical artery, or the concentrations of progesterone in maternal venous or umbilical arterial plasma. Our data on anencephalic fetal monkeys compare well with data available for human anencephaly and indicate that the fetal pituitary-adrenal axis in subhuman primates is involved in the normal timing of parturition and is important for the maintenance of normal maternal estradiol levels. Our data do not support the hypothesis that fetal cortisol initiates parturition in primates, but they do suggest that estrogens play a role in the initiation of parturition.